Pattern differences between newborn and adult rats in cisplatin-induced hepatorenal toxicity

Fulco, Bruna C.W.; Jung, Juliano Ten Kathen; Chagas, Pietro Maria; Quines, Caroline Brandão; Nogueira, Cristina Wayne; Zeni, Gilson

doi:10.1016/j.cbi.2018.08.011

Cited by 5 publications

(1 citation statement)

References 43 publications

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“…is used for the treatment of several human . The hepatotoxicity of CDDP is the major side effect of this drug which occurred during high doses treatment [24,25]. The present study sheds light on the possible protective effects of VST on CDDP -induced .…”

Section: Discussionmentioning

confidence: 59%

Antioxidant Traits and Protective Impact of Vorinostat against Cisplatin Induced Hepatoxicity in Rats

Kawy

Bashraf

Ali

et al. 2020

JPRI

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Background and Aim: Cisplatin "cis diamminedichloroplatinum [II] (CDDP) is the most widely used drug in cancer chemotherapy and hepatotoxicity is one of its major side effects. Vorinostat (VST) has been recognized to have an antioxidant and anti-inflammatory effect in low doses. The present study aimed to explore the potential protective effects of low dose VST against CDDP induced-liver toxicity in male Wistar rats. Methods: The rats were randomly divided into 4 groups (10 rats each); I-control group, II-CDDP group (7.5 mg/kg I.P. single dose 5 days before the end of the experiment) III-, VST group (15 mg/kg/day by gastric gavage for 28 days) and IV-CDDP + VST group (as in group II & III). Blood and livers samples were collected at the day 28th for biochemical and histopathological examinations. Results: Administration of CDDP significantly decrease hepatic GSH levels and increase serum alanine transaminase, aspartate transaminase and hepatic MDA, p53, TNF-α, and NF-κB levels compared to control. Pretreatment with VST significantly attenuated all unfavorable changes in these parameters. Histopathological analysis showed that VST significantly decreased liver inflammatory and degenerative changes induced by CDDP. VST also significantly increased Bcl-2 and decreased Caspas-3 immunoexpression in hepatic tissues. Conclusion: VST alleviates CDDP induced hepatic toxicity in rats by modulating MDA, p53, TNF-α, and NF-κB. It also significantly increased Bcl-2 and decreased Caspase-3.

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Section: Discussionmentioning

confidence: 59%

Antioxidant Traits and Protective Impact of Vorinostat against Cisplatin Induced Hepatoxicity in Rats

Kawy

Bashraf

Ali

et al. 2020

JPRI

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Reduction‐Sensitive Fluorinated‐Pt(IV) Universal Transfection Nanoplatform Facilitating CT45‐Targeted CRISPR/dCas9 Activation for Synergistic and Individualized Treatment of Ovarian Cancer

Zhang

et al. 2021

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Compared to traditional clustered regularly interspaced short palindromic repeat (CRISPR)/CRISPR‐associated protein 9 (Cas9) system, CRISPR/dead Cas9 (dCas9) system can precisely regulate endogenous gene expression without damaging the host gene, representing a greater potential for cancer therapy. Cancer/testis antigen 45 (CT45) is proved to enhance platinum‐based chemosensitivity for individualized ovarian cancer therapy. However, the development of a single nanocarrier codelivering CRISPR/dCas9 system and chemotherapeutics for synergistic cancer therapy still faces challenges. Herein, a reduction‐sensitive fluorinated‐Pt(IV) universal transfection nanoplatform (PtUTP‐F) is developed for the CT45‐targeted CRISPR/dCas9 activation to achieve synergistic and individualized treatment of ovarian cancer. Overcoming multiple physiological barriers, PtUTP‐F condensed gene can efficiently transfect into different cells including 293T cells, A2780, SKOV3, A549, and A2780/cisplatin (DDP) cancer cells, which is superior to Lipofectamine 6000. With the responsive release of gene and Pt(II) in the intracellular reducing microenvironment, PtUTP‐F/dCas9‐CT45 can generate CRISPR/dCas9 activation of CT45 expression for protein phosphatase 4C (PP4C) activity inhibition to hinder the DNA repair pathway and thus enhances the sensitivity to Pt(II) drugs for individualized A2780 tumor therapy. The PtUTP‐F not only represents a powerful nanoplatform for CRISPR/dCas9 system delivery but also initiates a novel strategy for synergistic and individualized treatment of CRISPR/dCas9‐based gene therapy with chemotherapy.

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Cardamonin inhibits the growth of human osteosarcoma cells through activating P38 and JNK signaling pathway

Zhang

Yang²,

Huang³

et al. 2021

Biomedicine & Pharmacotherapy

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Pattern differences between newborn and adult rats in cisplatin-induced hepatorenal toxicity

Cited by 5 publications

References 43 publications

Antioxidant Traits and Protective Impact of Vorinostat against Cisplatin Induced Hepatoxicity in Rats

Antioxidant Traits and Protective Impact of Vorinostat against Cisplatin Induced Hepatoxicity in Rats

Reduction‐Sensitive Fluorinated‐Pt(IV) Universal Transfection Nanoplatform Facilitating CT45‐Targeted CRISPR/dCas9 Activation for Synergistic and Individualized Treatment of Ovarian Cancer

Cardamonin inhibits the growth of human osteosarcoma cells through activating P38 and JNK signaling pathway

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